In many neurologic disorders, injury to neurons may be causedat least in part by overstimulation of receptors for excitatoryamino acids, including glutamate and aspartate. These neurologicconditions range from acute insults such as stroke, hypoglycemia,trauma, and epilepsy (Table 1) to chronic neurodegenerativestates such as Huntington's disease, the acquired immunodeficiencysyndrome (AIDS) dementia complex, amyotrophic lateral sclerosis,and perhaps Alzheimer's disease (Table 2)1,2,3.
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Table 1. Acute Neurologic Disorders Thought to Be Mediated at Least in Part through Stimulation of Glutamate Receptors.
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Table 2. Chronic Neurodegenerative Diseases Thought to Be Mediated at Least in Part through Stimulation . . . [Full Text of this Article]
Types of Excitatory Amino Acid Receptors
Intracellular Calcium and Neurotoxicity
Pathogenesis of Excitotoxicity
Mechanisms of Abnormal Glutamate Accumulation
Glutamate Transport
Release of Glutamate from Vesicular Stores
Injury and Glutamate Release
Role of Energy Failure in Neuronal Injury
Pathophysiology of Excitotoxicity at the Receptor Level
Potentiation of Postsynaptic Glutamate Responses
Pharmacotherapy for Excitatory Amino Acid-Induced Neurologic Disorders
Possible Sites of Action
NMDA Open-Channel Blockers
NMDA Redox Modulatory Site
Drugs Recently Approved and Clinical Trials in Progress
Conclusions
Source Information
From the Harvard-Longwood Neurology Program and the Laboratory of Cellular and Molecular Neuroscience, Department of Neurology, Children's Hospital (S.A.L., P.A.R.); the Departments of Neurology, Beth Israel Hospital, Brigham and Women's Hospital, and Massachusetts General Hospital (S.A.L.); and Harvard Medical School (S.A.L., P.A.R.) -- all in Boston.
Address reprint requests to Dr. Lipton at the Harvard-Longwood Neurology Program, 300 Longwood Ave., Enders Bldg., Suite 361, Boston, MA 02115.
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